Serotonin Enhances EPSP Amplitudes via the Release of Calcium Stores at IP₃ Receptor Sites and 2-APB Inhibits these Receptors and Decreases EPSP Amplitudes at the Crayfish Neuromuscular Junction

Abstract

Serotonin induces the release of internal calcium stores in the superficial extensor muscle of the crayfish neuromuscular junction. Inositol 1,4,5-trisphosphate (IP₃) and ryanodine receptor sites have both been implicated as the principal receptor for internal calcium. This study attempted to isolate and interpret the activity at IP₃ receptor sites by enhancing calcium release with serotonin (5-HT) and then inhibiting IP₃ receptors with the chemical 2- Aminoethoxydiphenyl borate (2-APB). We predicted that 5-HT would enhance excitatory postsynaptic potential (EPSP) amplitudes and the addition of 2-APB would mitigate this effect. This would imply that IP₃ receptors are the principal internal calcium receptors when the cell is exposed to 5-HT. Results were significant, mostly supporting our hypothesis. The data indicate that IP₃ receptors are the principal site of serotonin-induced calcium release but other sites and mechanisms are most likely also involved in this process. There is a need for variation in methods and approaches in this type of research to better understand the role of IP₃ receptors in the release of internal calcium stores.